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首页> 外文期刊>Neuroreport >Cell activation and inflammatory response following traumatic axonal injury in the rat.
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Cell activation and inflammatory response following traumatic axonal injury in the rat.

机译:大鼠轴突损伤后的细胞活化和炎症反应。

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摘要

In a rat model of traumatic brain injury cell activation was characterized immunohistochemically from 2 h up to 2 weeks. Reactive astrocytosis became apparent perivascularly and in the grey matter within 4h after trauma. Increased OX42 immunoreactivity indicated microglial activation in cortex and hippocampus as early as 4 h, whereas up-regulation of MHC class II (OX6) was evident in white matter tracts at 24 h. Although macrophage (ED1) numbers increased in the meninges and perivascularly, brain infiltration appeared marginal. Accumulation of lymphocytes and granulocytes was not observed. Our results show that traumatic axonal injury induces a rapid and sustained glial activation in the absence of leukocyte infiltration. Thus, cell activation following diffuse trauma strongly differs from that found after focal brain damage, awaiting further functional characterization.
机译:在大鼠颅脑损伤模型中,从2小时到2周以免疫组织化学方法表征了细胞活化。创伤后4小时内,反应性星形细胞增多在血管周围和灰质中变得明显。 OX42免疫反应性的增加表明皮层和海马中的小胶质细胞激活最早在4 h时出现,而II类MHC(OX6)的上调在24 h时很明显。尽管在脑膜和血管周巨噬细胞(ED1)数​​量增加,但脑浸润显得微不足道。没有观察到淋巴细胞和粒细胞的积累。我们的结果表明,在缺乏白细胞浸润的情况下,创伤性轴突损伤诱导了快速持续的胶质细胞活化。因此,弥漫性创伤后的细胞活化与局灶性脑损伤后的细胞活化有很大不同,有待进一步的功能表征。

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